{"title":"超高剂量率(FLASH)碳离子辐照抑制Pan02细胞株免疫抑制蛋白的表达。","authors":"Shohei Katsuki, Kazumasa Minami, Karin Oniwa, Masashi Yagi, Shinichi Shimizu, Noriaki Hamatani, Masaaki Takashina, Tatsuaki Kanai, Kazuhiko Ogawa","doi":"10.1093/jrr/rrae091","DOIUrl":null,"url":null,"abstract":"<p><p>Recently, ultra-high dose rate (> 40 Gy/s, uHDR; FLASH) radiation therapy (RT) has attracted interest, because the FLASH effect that is, while a cell-killing effect on cancer cells remains, the damage to normal tissue could be spared has been reported. This study aimed to compare the immune-related protein expression on cancer cells after γ-ray, conventionally used dose rate (Conv) carbon ion (C-ion), and uHDR C-ion. B16F10 murine melanoma and Pan02 murine pancreas cancer were irradiated with γ-ray at Osaka University and with C-ion at Osaka HIMAK. The dose rates at 1.16 Gy/s for Conv and 380 Gy/s for uHDR irradiation. The expressed calreticulin (CRT), major histocompatibility complex class (MHC)-I, and programmed cell death 1 ligand (PD-L1) were evaluated by flow cytometry. Western blotting and PCR were utilized to evaluate endoplasmic reticulum (ER) stress, DNA damage, and its repair pathway. CRT, MHC-I on B16F10 was also increased by irradiation, while only C-ion increased MHC-I on Pan02. Notably, PD-L1 on B16F10 was increased after irradiation with both γ-ray and C-ion, while uHDR C-ion suppressed the expression of PD-L1 on Pan02. The present study indicated that uHDR C-ion has a different impact on the repair pathway of DNA damage and ER than the Conv C-ion. This is the first study to show the immune-related protein expressions on cancer cells after uHDR C-ion irradiation.</p>","PeriodicalId":16922,"journal":{"name":"Journal of Radiation Research","volume":" ","pages":"97-102"},"PeriodicalIF":1.9000,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Ultra-high dose rate (FLASH) carbon ion irradiation inhibited immune suppressive protein expression on Pan02 cell line.\",\"authors\":\"Shohei Katsuki, Kazumasa Minami, Karin Oniwa, Masashi Yagi, Shinichi Shimizu, Noriaki Hamatani, Masaaki Takashina, Tatsuaki Kanai, Kazuhiko Ogawa\",\"doi\":\"10.1093/jrr/rrae091\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Recently, ultra-high dose rate (> 40 Gy/s, uHDR; FLASH) radiation therapy (RT) has attracted interest, because the FLASH effect that is, while a cell-killing effect on cancer cells remains, the damage to normal tissue could be spared has been reported. This study aimed to compare the immune-related protein expression on cancer cells after γ-ray, conventionally used dose rate (Conv) carbon ion (C-ion), and uHDR C-ion. B16F10 murine melanoma and Pan02 murine pancreas cancer were irradiated with γ-ray at Osaka University and with C-ion at Osaka HIMAK. The dose rates at 1.16 Gy/s for Conv and 380 Gy/s for uHDR irradiation. The expressed calreticulin (CRT), major histocompatibility complex class (MHC)-I, and programmed cell death 1 ligand (PD-L1) were evaluated by flow cytometry. Western blotting and PCR were utilized to evaluate endoplasmic reticulum (ER) stress, DNA damage, and its repair pathway. CRT, MHC-I on B16F10 was also increased by irradiation, while only C-ion increased MHC-I on Pan02. Notably, PD-L1 on B16F10 was increased after irradiation with both γ-ray and C-ion, while uHDR C-ion suppressed the expression of PD-L1 on Pan02. The present study indicated that uHDR C-ion has a different impact on the repair pathway of DNA damage and ER than the Conv C-ion. This is the first study to show the immune-related protein expressions on cancer cells after uHDR C-ion irradiation.</p>\",\"PeriodicalId\":16922,\"journal\":{\"name\":\"Journal of Radiation Research\",\"volume\":\" \",\"pages\":\"97-102\"},\"PeriodicalIF\":1.9000,\"publicationDate\":\"2025-01-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Radiation Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/jrr/rrae091\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Radiation Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/jrr/rrae091","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
近年来,超高剂量率(40gy /s, uHDR;闪光(FLASH)放射疗法(RT)引起了人们的兴趣,因为有报道称,闪光效应(FLASH effect)在对癌细胞产生细胞杀伤作用的同时,可以避免对正常组织的损害。本研究旨在比较γ射线、常规剂量率(Conv)碳离子(C-ion)和uHDR c -离子对肿瘤细胞免疫相关蛋白表达的影响。在大阪大学用γ射线照射B16F10小鼠黑色素瘤和Pan02小鼠胰腺癌,在大阪HIMAK用c离子照射。Conv的剂量率为1.16 Gy/s, uHDR的剂量率为380 Gy/s。流式细胞术检测钙调蛋白(CRT)、主要组织相容性复合体类(MHC)-I和程序性细胞死亡1配体(PD-L1)的表达。Western blotting和PCR检测内质网应激、DNA损伤及其修复途径。CRT照射后,B16F10上的MHC-I也增加,而Pan02上只有c离子增加MHC-I。值得注意的是,γ射线和c离子辐照后,B16F10上的PD-L1均升高,而uHDR c离子则抑制了Pan02上PD-L1的表达。本研究表明,uHDR c -离子对DNA损伤和ER修复途径的影响不同于Conv c -离子。这是首次研究uHDR c离子辐照后癌细胞免疫相关蛋白的表达。
Ultra-high dose rate (FLASH) carbon ion irradiation inhibited immune suppressive protein expression on Pan02 cell line.
Recently, ultra-high dose rate (> 40 Gy/s, uHDR; FLASH) radiation therapy (RT) has attracted interest, because the FLASH effect that is, while a cell-killing effect on cancer cells remains, the damage to normal tissue could be spared has been reported. This study aimed to compare the immune-related protein expression on cancer cells after γ-ray, conventionally used dose rate (Conv) carbon ion (C-ion), and uHDR C-ion. B16F10 murine melanoma and Pan02 murine pancreas cancer were irradiated with γ-ray at Osaka University and with C-ion at Osaka HIMAK. The dose rates at 1.16 Gy/s for Conv and 380 Gy/s for uHDR irradiation. The expressed calreticulin (CRT), major histocompatibility complex class (MHC)-I, and programmed cell death 1 ligand (PD-L1) were evaluated by flow cytometry. Western blotting and PCR were utilized to evaluate endoplasmic reticulum (ER) stress, DNA damage, and its repair pathway. CRT, MHC-I on B16F10 was also increased by irradiation, while only C-ion increased MHC-I on Pan02. Notably, PD-L1 on B16F10 was increased after irradiation with both γ-ray and C-ion, while uHDR C-ion suppressed the expression of PD-L1 on Pan02. The present study indicated that uHDR C-ion has a different impact on the repair pathway of DNA damage and ER than the Conv C-ion. This is the first study to show the immune-related protein expressions on cancer cells after uHDR C-ion irradiation.
期刊介绍:
The Journal of Radiation Research (JRR) is an official journal of The Japanese Radiation Research Society (JRRS), and the Japanese Society for Radiation Oncology (JASTRO).
Since its launch in 1960 as the official journal of the JRRS, the journal has published scientific articles in radiation science in biology, chemistry, physics, epidemiology, and environmental sciences. JRR broadened its scope to include oncology in 2009, when JASTRO partnered with the JRRS to publish the journal.
Articles considered fall into two broad categories:
Oncology & Medicine - including all aspects of research with patients that impacts on the treatment of cancer using radiation. Papers which cover related radiation therapies, radiation dosimetry, and those describing the basis for treatment methods including techniques, are also welcomed. Clinical case reports are not acceptable.
Radiation Research - basic science studies of radiation effects on livings in the area of physics, chemistry, biology, epidemiology and environmental sciences.
Please be advised that JRR does not accept any papers of pure physics or chemistry.
The journal is bimonthly, and is edited and published by the JRR Editorial Committee.